Scientists have delved more deeply into the evolutionary history of the fruit fly than ever before to reveal the genetic activity that led to the development of wings – a key to the insect’s ability to survive. The wings themselves are common research models for this and other species’ appendages. But until now, scientists did not know how the fruit fly,Drosophila melanogaster, first sprouted tiny buds that became flat wings. A cluster of only 20 or so cells present in the fruit fly’s first day of larval life was analyzed to connect a gene known to be active in the embryo and the gene that triggers the growth of wings. Researchers determined that the known embryonic gene, called Dpp, sends the first signal to launch the activation of a gene called vn. That signal alone is dramatic, because it crosses cell layers. The activation of the vn gene lasts just long enough to turn on a target gene that combines with additional signals to activate genes responsible for cell growth and completion of wing development. “Our work shows how when you add a gene into the equation, you get a wing. The clue is that one growth factor, Dpp, turns on another growth factor, vn, but just for a short period of time. You absolutely need a pulse of this activity to turn on yet another gene cascade that gives you a wing, but if vn is active for too long, a wing wouldn’t form,” said Dr. Amanda Simcox, professor of molecular genetics at The Ohio State University and lead author of the study. “We learned all this from investigating 20 tiny cells. The events could be responsible for this big event in evolutionary history, when the insect got its wing.

New research shows that a tiny piece of RNA has an essential role in ensuring that embryonic tissue segments form properly. The study, conducted in chicken embryos, determined that this piece of RNA regulates cyclical gene activity that defines the timing of the formation of tissue segments that later become muscle and vertebrae. Genes involved in this activity are turned on and off in an oscillating pattern that matches the formation of each tissue segment. If the timing of these genes’ activity doesn’t remain tightly regulated, the tissue either won’t form at all or will form with defects. One gene long associated with this segmentation “clock” is called Lfng. Researchers established in this study that a single microRNA – a tiny segment of RNA that has no role in producing any protein – is key to turning off Lfng at precisely the right time as tissues form in this oscillating pattern. When the microRNA was deleted or manipulated so that it wouldn’t bind when it was supposed to, the oscillatory pattern of the genetic clock was broken and tissue development was abnormal. “It’s a big deal to find that a single interaction between a microRNA and its target has this very profound effect when you interfere with its function,” said Dr. Susan Cole, associate professor of molecular genetics at The Ohio State University and lead author of the study. “There are very few cases where interfering with just one microRNA during development can make this much of a difference. But here, this regulation is so tight that this turns out to be incredibly important.